Testicular germ cell tumours (TGCTs) are the most common malignancy and the leading cause of death from solid tumours in young men. 1,2 These tumours peak during the third decade of life, and an increasing incidence has been reported widely. 3 Histologically, TGCTs are subdivided into various elements. Type II TGCT refers to seminomas and non-seminomas of (predominantly) adolescents

The role of TDRG1 in tumorigenesis and the progression of seminoma, as well as its role in regulating chemosensitivity of seminoma to cisplatin through the PI3K/Akt/mTOR signaling pathway, has been previously defined. However, the detailed mechanism underlying TDRG1 expression and concomitant chemoresistance conditions are unknown. Furthermore, it has been reported that non‐protein‐coding RNAs play an important role in a variety of vital processes including cellular chemosensitivity. However, the role of non‐protein‐coding RNAs in regulating the chemosensitivity of seminoma remains unknown. In this study, using microarray analysis, we found that long non‐coding RNA H19 was upregulated while miRNA‐106b‐5p was downregulated in an established cisplatin‐resistant TCam‐2 cell line. Moreover, H19 acts as a miRNA‐106b‐5p sponge and thus impairs the function of miRNA‐106b‐5p on its target gene, TDRG1. Based on these findings, we propose that H19 promotes the expression of TDRG1 by sequestering miRNA‐106b‐5p and uses this mechanism to facilitate cell survival in cisplatin‐based chemotherapeutic conditions. These findings elucidate the mechanisms, at least partially, applied to deregulate TDRG1 and cisplatin sensitivity, and may provide new therapeutic possibilities for chemoresistant seminoma.

MicroRNA (miRNA)-gene interactions are well-recognized as involved in the progression of almost all cancer types including prostate cancer, which is one of the most common cancers in men. This study explored the significantly dysregulated genes and miRNAs and elucidated the potential miRNA-gene regulatory network in prostate cancer. Integrative analysis of prostate cancer and normal prostate transcriptomic data in The Cancer Genome Atlas dataset was conducted using both differential expression analysis and weighted correlation network analysis (WGCNA). Thirteen genes (RRM2,

BackgroundThe purpose of this study aimed to assess preoperative risk factors for the incidence of deep venous thromboembolism in patients undergoing posterior lumbar interbody fusion (PLIF).MethodsThe diagnosis of preoperative deep vein thrombosis (DVT) was confirmed by Doppler ultrasonography. To examine the preoperative risk factors for DVT admitted for PLIF, comparative analysis of the DVT-positive and DVT-negative groups was done.ResultsDVT was detected in 9.4 % (269/2861) patients, including 17 proximal DVT patients (6.3 %) and 252 the distal DVT patients (93.7 %). According to multivariate logistic regression analysis, the age, preoperative D-dimer, and history of rheumatoid arthritis were significant risk factors relative to the onset of DVT after posterior lumbar surgery.ConclusionsAccording to the result of our study, age, positive preoperative plasma D-dimer level, and rheumatoid arthritis had the influential impact on the incidence of DVT admitted for PLIF.

The clear cell renal cell carcinoma (ccRCC) microenvironment consists of many different cell types and structural components that play critical roles in cancer progression and drug resistance, but the cellular architecture and underlying gene regulatory features of ccRCC have not been fully characterized. Here, we applied single-cell RNA sequencing (scRNA-seq) and single-cell assay for transposase-accessible chromatin sequencing (scATAC-seq) to generate transcriptional and epigenomic landscapes of ccRCC. We identified tumor cell-specific regulatory programs mediated by four key transcription factors (TFs) (HOXC5, VENTX, ISL1, and OTP), and these TFs have prognostic significance in The Cancer Genome Atlas (TCGA) database. Targeting these TFs via short hairpin RNAs (shRNAs) or small molecule inhibitors decreased tumor cell proliferation. We next performed an integrative analysis of chromatin accessibility and gene expression for CD8+ T cells and macrophages to reveal the different regulatory elements in their subgroups. Furthermore, we delineated the intercellular communications mediated by ligand–receptor interactions within the tumor microenvironment. Taken together, our multiomics approach further clarifies the cellular heterogeneity of ccRCC and identifies potential therapeutic targets.